A-S.B.16: A Mathematical Model for the Co-regulation of Antiviral and Inflammatory Genes Mediated by NF-κB and IRF-3 post Viral Infections
Rajiv Kumar Mishra
iOligos Technologies Pvt. Ltd.,Noida
Soumen Basak
National Institute of Immunology, New Delhi
Rakesh Pandey
MMV, Banaras Hindu University
Keywords
Viral Infection, Systems Biology, Immune Systems, Inflammation, Modeling of Biological Systems
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The anti-viral and inflammatory responses of host cells are activated through several signalling pathways, such as NF-κB, IRF-3 and IRF-7 in response to viral infections. These transcription factors regulate the expression of antiviral genes that encode type I interferons (IFNα/β). However, the exact mechanism underlying the complex context-dependent temporal activation of IFNα/β remains unclear. Here, we have developed a probability-based mathematical model to study the co-activation of the IFNβ gene by NF-κB and IRF-3. Our model results suggest that the rapid and elevated as well as a delayed but persistent expression of IFNβ would be observed due to a temporal bias in the binding of NF-κB and IRF-3, highlighting the need for co-regulation of IFNβ by two different signalling pathways. In addition, the model predicts that the binding affinity of NF-κB to the promoter of IFNβ would be equal to or greater than that of IRF-3 for a quick, strong and persistent antiviral response.
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